Extracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarction
Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascul...
Main Authors: | , , , , , , , , , , , , , , , , , , , , |
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Format: | Journal article |
Language: | English |
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Elsevier
2023
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_version_ | 1797113265769152512 |
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author | Hardy, SA Liesinger, L Patrick, R Poettler, M Rech, L Gindlhuber, J Mabotuwana, NS Ashour, D Stangl, V Bigland, M Murtha, LA Starkey, MR Scherr, D Hansbro, PM Hoefler, G Ramos, G Cochain, C Harvey, RP Birner-Gruenberger, R Boyle, AJ Rainer, PP |
author_facet | Hardy, SA Liesinger, L Patrick, R Poettler, M Rech, L Gindlhuber, J Mabotuwana, NS Ashour, D Stangl, V Bigland, M Murtha, LA Starkey, MR Scherr, D Hansbro, PM Hoefler, G Ramos, G Cochain, C Harvey, RP Birner-Gruenberger, R Boyle, AJ Rainer, PP |
author_sort | Hardy, SA |
collection | OXFORD |
description | Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascular cells in uninjured human and mouse hearts, and from M1 and M2 macrophages and myofibroblasts after MI. ECM-1 stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic and inflammatory pathways, and inhibits cardiac fibroblast migration. ECM-1 binds HuCFb cell surface receptor LRP1, and LRP1 inhibition blocks ECM-1 from stimulating fibroblast-to-myofibroblast transition, confirming a novel ECM-1-LRP1 fibrotic signaling axis. ECM-1 may represent a novel mechanism facilitating inflammation-fibrosis crosstalk. |
first_indexed | 2024-03-07T08:03:52Z |
format | Journal article |
id | oxford-uuid:9999a5b8-581c-4276-961d-2b14cb1a428f |
institution | University of Oxford |
language | English |
last_indexed | 2024-04-23T08:26:05Z |
publishDate | 2023 |
publisher | Elsevier |
record_format | dspace |
spelling | oxford-uuid:9999a5b8-581c-4276-961d-2b14cb1a428f2024-04-15T09:31:18ZExtracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarctionJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:9999a5b8-581c-4276-961d-2b14cb1a428fEnglishSymplectic ElementsElsevier2023Hardy, SALiesinger, LPatrick, RPoettler, MRech, LGindlhuber, JMabotuwana, NSAshour, DStangl, VBigland, MMurtha, LAStarkey, MRScherr, DHansbro, PMHoefler, GRamos, GCochain, CHarvey, RPBirner-Gruenberger, RBoyle, AJRainer, PPIrreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascular cells in uninjured human and mouse hearts, and from M1 and M2 macrophages and myofibroblasts after MI. ECM-1 stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic and inflammatory pathways, and inhibits cardiac fibroblast migration. ECM-1 binds HuCFb cell surface receptor LRP1, and LRP1 inhibition blocks ECM-1 from stimulating fibroblast-to-myofibroblast transition, confirming a novel ECM-1-LRP1 fibrotic signaling axis. ECM-1 may represent a novel mechanism facilitating inflammation-fibrosis crosstalk. |
spellingShingle | Hardy, SA Liesinger, L Patrick, R Poettler, M Rech, L Gindlhuber, J Mabotuwana, NS Ashour, D Stangl, V Bigland, M Murtha, LA Starkey, MR Scherr, D Hansbro, PM Hoefler, G Ramos, G Cochain, C Harvey, RP Birner-Gruenberger, R Boyle, AJ Rainer, PP Extracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarction |
title | Extracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarction |
title_full | Extracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarction |
title_fullStr | Extracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarction |
title_full_unstemmed | Extracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarction |
title_short | Extracellular matrix protein-1 as a mediator of inflammation-induced fibrosis after myocardial infarction |
title_sort | extracellular matrix protein 1 as a mediator of inflammation induced fibrosis after myocardial infarction |
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